The mitral annulus represents the junction of the fibrous and muscular tissue that joins the left atrium and the left ventricle. The mitral valve is a bicuspid valve having a relatively large anterior leaflet that coapts or meets with a smaller posterior leaflet.
FIG. 1 illustrates a normal mitral heart valve 14 from the left atrium from a surgical view of the heart. The anterior portion A of the mitral annulus 15 forms a part of the “cardiac skeleton” and is bounded by anterior and posterior commissures 16, 17. The anterior commissure 16 and posterior commissure 17 are generally at the junction points of the anterior leaflet 18 and the posterior leaflet 19. The junction points are also known as the anterolateral commissure 16 and posteromedial commissure 17. The posterior portion P of the mitral annulus 15 consists mainly of muscular tissue of the outer wall of the heart.
Referring to FIGS. 1 and 2, posterior leaflet 19 is divided into three scallops indicated as P1, P2, and P3 in sequence from the anterior commissure 16 counterclockwise to the posterior commissure 17. Anterior leaflet 18 is also divided into three areas indicated as A1, A2, and A3 in sequence from the anterior commissure 16 clockwise to the posterior commissure 17.
Ischemic heart disease can cause a mitral valve to become incompetent. In patients who suffer from cardiomyopathy due to ischemia, regions of the left ventricle lose their contractility and dilate. As the disease progresses, the left ventricle enlarges and becomes more round in shape, going from a conical shape to more of a spherical shape. Referring to FIG. 2, papillary muscles 23, 25 are displaced down (inferiorly) and away from each other. The change in the location of the papillary muscles increases the distance between the papillary muscles and the mitral valve annulus. This creates tension on the chordae tendonae 21 that connect the posterior papillary muscle 23 to the mitral valve leaflets in the A2, A3, P2, and P3 regions of the annulus. Since the chordae tendonae 21 do not change their length significantly, the chordae 21 tend to pull or “tether” the mitral leaflets. In severe cases of left ventricle dilation, the tethering of the chordae prevents the leaflets from coming together or coapting correctly, resulting in mitral valve regurgitation. In addition to remodeling of the left ventricle, the mitral valve tends to flatten during ventricular systole instead of achieving its natural saddle shape. This also disrupts the natural coaptation of the mitral leaflets and the natural distribution of stresses over the leaflets and chordae tendonae.
In ischemic mitral regurgitation (IMR), the entire circumference of the mitral annulus may dilate. The posterior portion of the annulus may dilate more than the anterior portion because the anterior portion has more support from the heart's fibrous skeleton. In cases where IMR is caused by posteromedial myocardial infarction, there may be an asymmetric dilation of the posteromedial annulus, which is indicated at A2, A3, P2, and P3. In this case, the IMR may be caused by tethering of leaflet segments connected to the posteromedial papillary muscle. This is often in the A2, A3, P2, and P3 segments of the mitral valve.
Often, this type of mitral valve regurgitation is surgically repaired with an annuloplasty ring (which may be either a complete ring or a C-shaped “ring” with an opening along the anterior side). The repair restores proper leaflet coaptation by decreasing the diameter of the mitral valve annulus, thereby mitigating the effect of the tethering of the chordae and the effects of dilation of the annulus. One surgical correction for IMR is to tether the posteromedial annulus of the mitral valve to the posteromedial papillary muscle. This papillary muscle relocation procedure reduces the chordal tension and allows the leaflets to coapt more effectively.